2-Deoxy-D-glucose (2-DG) - 10mM in DMSO, high purity , CAS No.154-17-6(DMSO)

Item Number

D408100

• Specifications & Purity: 10mM in DMSO
• Biochemical and Physiological Mechanisms: 2-Deoxy-D-glucose (2-DG, 2-deoxyglucose, NSC 15193, 2-Deoxy-D-arabino-hexose, D-Arabino-2-deoxyhexose), an analog of glucose, is a glycolytic inhibitor with antiviral activity. 2-Deoxy-D-glucose induces apoptosis and inhibits Herpes Simplex Virus type-1 (
• Storage Temp: Store at -80°C
• Shipped In: Ice chest + Ice pads

Product Description

Information

2-Deoxy-D-glucose (2-DG) 2-Deoxy-D-glucose (2-DG, 2-deoxyglucose, NSC 15193, 2-Deoxy-D-arabino-hexose, D-Arabino-2-deoxyhexose), an analog of glucose, is a glycolytic inhibitor with antiviral activity. 2-Deoxy-D-glucose induces apoptosis and inhibits He
In vitro

2-Deoxy-D-glucose(2-DG) activates AKT function through phosphatidylinositol 3-kinase (PI3K) and is independent of glycolysis or mTOR inhibition. 2-DG treatments disrupts the binding between insulin-like growth factor 1 (IGF-1) and IGF-binding protein 3 (IGFBP3) so that the free form of IGF-1 could be released from the IGF-1·IGFBP3 complex to activate IGF-1 receptor (IGF1R) signaling. 2-DG-induced activation of many survival pathways can be jointly attenuated through IGF1R inhibition. 2-DG also induces time- and dose-dependent ERK phosphorylation. 2-DG is readily transported into cells and is phosphorylated by hexokinase, but cannot be metabolized further and accumulates in the cell. This leads to ATP depletion and the induction of cell-death. 2DG significantly suppresses proliferation, causes apoptosis and reduces migration of murine endothelial cells, inhibiting formation of lamellipodia and filopodia and causing disorganization of F-actin filaments in murine endothelial cell.

In vivo

Treatment of cancer patients with relatively high doses of 2-DG (greater than 200 mg/kg) was largely ineffective in managing tumor growth. Side effects of 2-DG included elevated blood glucose levels, progressive weight loss with lethargy, and behavioral symptoms of hypoglycemia. 2-DG enhances isoflurane-induced loss of righting reflex in mice. By reducing metabolism, 2-DG treatment can decrease body temperature in rodent, enhancing sensitivity to anesthetics. 2-DG diet significantly increased serum ketone body level and brain expression of enzymes required for ketone body metabolism. The 2-DG-induced maintenance of mitochondrial bioenergetics was paralleled by simultaneous reduction in oxidative stress. Further, 2-DG treated mice exhibited a significant reduction of both amyloid precursor protein (APP) and amyloid beta (Aβ) oligomers, which was paralleled by significantly increased α-secretase and decreased γ-secretase expression, indicating that 2-DG induced a shift towards a non-amyloidogenic pathway. 2-DG increased expression of genes involved in Aβ clearance pathways, degradation, sequestering, and transport. Concomitant with increased bioenergetic capacity and reduced β-amyloid burden, 2-DG significantly increased expression of neurotrophic growth factors, BDNF and NGF, thus reduces pathology in female mouse model of Alzheimer\'s disease.
Cell Data

cell lines：BT20, U87MG, and SKOV3 cells

Concentrations：5 mM

Incubation Time：48 h

Powder Purity: